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Neurological Disorders

Our Neurological section contains a wide range of medications that can be used to treat various neurological disorders, including Alzheimer’s, epilepsy, migraine and Parkinson’s disease, as well as other conditions with a neurological basis like motion sickness.

The different classes of Neurological medication are listed on the left of the page and when you click on one of these, the principal brand name products display in the left column and generic alternatives to the right.

Use the search feature to quickly find the product you are looking for, by entering either the active ingredient, e.g. carbamazepine or the product name, e.g. Tegretol.

Our Neurological section contains a wide range of medications that can be used to treat various neurological disorders, including Alzheimer’s, epilepsy, migraine and Parkinson’s disease, as well as other conditions with a neurological basis like motion sickness.

The different classes of Neurological medication are listed on the left of the page and when you click on one of these, the principal brand name products display in the left column and generic alternatives to the right.

Use the search feature to quickly find the product you are looking for, by entering either the active ingredient, e.g. carbamazepine or the product name, e.g. Tegretol.

Scopoderm TTSScopolaminePatches used in travel/sea sicknessFrom $13.50 per Patch

What is motion sickness?

Motion sickness is associated with various forms of travel including air, sea, train or car travel. It is also possible to experience motion sickness when watching a movie in which dramatic movements are shown, but the body is motionless. Movement is detected by the vestibular system of the ear, which comprise the fluid filled canals in the inner ear. These detect motion or changes in the body’s position and send the information to the brain. If visual messages sent by the eye suggest that the body is still, this conflict causes the brain to interpret this discrepancy as an hallucination due to an ingested toxin that needs to be cleared from the system. This stimulates the area postrema of the brain to induce the vomiting reflex. Motion sickness is a neurological condition that is based on perception rather than a physical disorder.

How do antiemetics help with motion sickness?

Antiemetics like the anticholinergic scopolamine work by blocking specific receptors for acetylcholine in the vestibular system of the ear and in the brain. Stimulation of acetylcholine receptors is involved in the transmission of information from the vestibular system of the ear to the vomiting center in brain and from the brain to the stomach. The anticholinergic action of antiemetics like scopolamine prevents the vomiting reflex from being induced, which eases symptoms of motion sickness.
...Read more

What is motion sickness?

Motion sickness is associated with various forms of travel including air, sea, train or car travel. It is also possible to experience motion sickness when watching a movie in which dramatic movements are shown, but the body is motionless. Movement is detected by the vestibular system of the ear, which comprise the fluid filled canals in the inner ear. These detect motion or changes in the body’s position and send the information to the brain. If visual messages sent by the eye suggest that the body is still, this conflict causes the brain to interpret this discrepancy as an hallucination due to an ingested toxin that needs to be cleared from the system. This stimulates the area postrema of the brain to induce the vomiting reflex. Motion sickness is a neurological condition that is based on perception rather than a physical disorder.

How do antiemetics help with motion sickness?

Antiemetics like the anticholinergic scopolamine work by blocking specific receptors for acetylcholine in the vestibular system of the ear and in the brain. Stimulation of acetylcholine receptors is involved in the transmission of information from the vestibular system of the ear to the vomiting center in brain and from the brain to the stomach. The anticholinergic action of antiemetics like scopolamine prevents the vomiting reflex from being induced, which eases symptoms of motion sickness.
...Read more

What is Alzheimer’s?

Alzheimer's Disease is the most common form of dementia among older people and is characterised by memory loss, language problems, personality changes and unpredictable behaviour. It is progressive and irreversible and as symptoms worsen it leads to a gradual decline in cognitive function, which covers thinking, reasoning and learning abilities. Changes in brain structure have been associated with the progression of Alzheimer's Disease. These changes involve the destruction of specific areas of the brain and degeneration of brain cells (neurones), particularly those that produce acetylcholine, a neurotransmitter that is continually released by brain cells in the regions of the inner temporal lobes which control cognitive function. Once released, acetylcholine is degraded by the enzyme cholinesterase to prevent its build up in the synapses, which are the gaps between neurones. As the disease progresses, abnormal structures appear in the brain, starting in the inner temporal lobes and the cerebral cortex and then spreading to other regions. These plaques of neurons and tangles of nerve fibres are associated with the damaging and killing of nerve cells, followed by loss of connections between neurones in the brain and loss of communication by neurotransmitters, which is linked with the gradual loss of memory and ability to understand, communicate and reason.

Medication for Alzheimer's

Medications that increase the amount of acetylcholine by preventing its destruction in areas of the brain affected by Alzheimer's Disease are used to help slow down the loss of cognitive function. These medications include rivastigmin and they work by inhibiting the action of cholinesterase that breaks down acetylcholine. This action slows down the degradation of acetylcholine released by acetylcholine-producing neurones that are still functional and this increases levels of acetylcholine in the damaged areas of the brain. Cholinesterase inhibitors help slow down the progression of mild to moderate Alzheimer's Disease and can improve the cognitive processes of thinking, learning and memory; and also reduce the personality and behavioural changes associated with Alzheimer's, which improves daily functioning in people living with Alzheimer's.
...Read more

What is Alzheimer’s?

Alzheimer's Disease is the most common form of dementia among older people and is characterised by memory loss, language problems, personality changes and unpredictable behaviour. It is progressive and irreversible and as symptoms worsen it leads to a gradual decline in cognitive function, which covers thinking, reasoning and learning abilities. Changes in brain structure have been associated with the progression of Alzheimer's Disease. These changes involve the destruction of specific areas of the brain and degeneration of brain cells (neurones), particularly those that produce acetylcholine, a neurotransmitter that is continually released by brain cells in the regions of the inner temporal lobes which control cognitive function. Once released, acetylcholine is degraded by the enzyme cholinesterase to prevent its build up in the synapses, which are the gaps between neurones. As the disease progresses, abnormal structures appear in the brain, starting in the inner temporal lobes and the cerebral cortex and then spreading to other regions. These plaques of neurons and tangles of nerve fibres are associated with the damaging and killing of nerve cells, followed by loss of connections between neurones in the brain and loss of communication by neurotransmitters, which is linked with the gradual loss of memory and ability to understand, communicate and reason.

Medication for Alzheimer's

Medications that increase the amount of acetylcholine by preventing its destruction in areas of the brain affected by Alzheimer's Disease are used to help slow down the loss of cognitive function. These medications include rivastigmin and they work by inhibiting the action of cholinesterase that breaks down acetylcholine. This action slows down the degradation of acetylcholine released by acetylcholine-producing neurones that are still functional and this increases levels of acetylcholine in the damaged areas of the brain. Cholinesterase inhibitors help slow down the progression of mild to moderate Alzheimer's Disease and can improve the cognitive processes of thinking, learning and memory; and also reduce the personality and behavioural changes associated with Alzheimer's, which improves daily functioning in people living with Alzheimer's.
...Read more

Transmission of nerve impulses

Messages are transmitted from one neurone (nerve cell) to another by the generation of electrical and chemical signals. At one end of the neurone, structures called dendrites pick up the stimulus from the connecting neurone and this generates an electrical signal that travels down the body of the cell called the axon and stimulates the release of chemical signals or neurotransmitters from the other end. These neurotransmitters travel across the gap or synapse between the axon terminal of one neurone (pre-synaptic) and the dendrites at the top of the next neurone (post-synaptic). They bind to specific receptors and trigger the generation of another electrical signal in the next neurone. This transmission of electrical and chemical messages takes just milliseconds to complete.

An electrical signal is generated by the exchange of charged particles or ions across voltage-dependant ion channels in the cell membrane controlled by ion pumps. When a neurone is not transmitting messages it is resting and its membrane is polarised which means that the electrical charge on the outside of the membrane is positive due to an excess of sodium ions, while the charge on the inside is negative and there is an excess of potassium ions.

When the neurone is stimulated, the gated channels on the membrane open and sodium ions flood into the cell and the membrane becomes depolarised generating an action potential and an electrical signal is propagated along the axon. The ions return to their original levels and the cell becomes repolarised, ready to receive another signal.

At the other end of the neurone, the electrical signal triggers the membrane to depolarise allowing calcium ions to enter the cell and this stimulates the release of neurotransmitters. Some neurotransmitters trigger an action potential in the next neurone and are is stimulatory, others are inhibitory and prevent the generation of an action potential. Once it has done its job the neurotransmitter is degraded or reabsorbed back into the pre-synaptic neurone that released it, so that the stimulus stops once transmission to the next neurone is complete.

What is epilepsy?

Epilepsy is characterised by recurring spontaneous seizures, which is uncontrolled muscular spasm, due to episodes of abnormal electrical activity in the brain. A chemical imbalance of neurotransmitters in the brain results in a malfunction in the transmission of electrical signals and causes repetitive firing and transmission of excitatory nerve messages. These bursts of abnormal electrical activity in the brain send nerve signals to the motor neurones in the central nervous system and trigger seizures. Epileptic seizures vary from mild convulsions to violent muscle spasms with loss of consciousness, depending on the part of the brain affected. The trigger for epileptic seizures can be due to anything that disturbs normal activity of neurones, including head injury, stroke, brain tumour, brain infection, drug abuse, but in many cases the cause is unknown (idiopathic) and epilepsy can start at any age.

Medications for epilepsy

Drugs used to prevent epileptic seizures are anticonvulsants that control the bursts of electrical activity in the brain that cause seizures. They work by preventing the repetitive firing of nerve messages acting through different mechanisms, including:

Blocking sodium channels that are involved in triggering the action potential and setting up the nerve signal

Blocking calcium channels that respond to the nerve signal and trigger the release of neurotransmitters

Adjusting the balance between inhibitory and excitatory neurotransmitters

Some medications work by more that one mechanism and act by a combination of these mechanisms.

Sodium/calcium channel blockers

Some anticonvulsants control neurotransmission and act directly on nerve cells to stabilise nerve cell membranes by blocking sodium or calcium channels. This reduces electrical activity and helps to “calm down” nerves that have become hyperexcited, thereby inhibiting the repetitive firing and transmission of excitatory nerve messages, in areas of the brain where hyperactivity causes seizures. Medications that act as membrane stabilisers include the following:

Carbamazepine blocks voltage-dependent sodium channels in nerve cell membranes that control the flow of sodium ions into the nerve cell and triggers an electrical transmission, which in hyperexcited nerve cells can trigger a seizure. This action is also thought to suppress the release of the neurotransmitters dopamine and noradrenaline.

Phenytoin acts directly on a specific area in the brain called the motor cortex, which controls movement and works by promoting the release of sodium ions out of the nerve cell through voltage-gated sodium channels in the membrane. This prevents the spread of electrical activity that sends nerve signals from the brain to the central nervous system to trigger a seizure.

Inhibitory and excitatory neurotransmitters

For the brain to function normally it is important to have a balance between excitatory and inhibitory neurotransmitters. Glutamate is the major excitatory neurotransmitter and interacts with receptors that have excitatory effects, which means that they increase the probability that the target cell will set up an action potential and trigger a nerve signal. Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter and interacts with receptors that have inhibitory effects by failing to trigger a nerve signal and this has a calming effect on nerve cells. Medications that regulate the balance between excitatory and inhibitory neurotransmitters include the following:

Sodium valproate increases the activity of the inhibitory neurotransmitter GABA. It works by inhibiting GABA degradative enzymes like GABA transaminase and/or succinic semialdehyde dehydrogenase thereby preventing its degradation; also by preventing the reuptake of GABA by the pre-synaptic nerve cell.

Topiramate stimulates the activity of GABA by enhancing the frequency that it activates its receptor; also by enhancing the ability of GABA to increase the flow of calcium ions into the end of the nerve cell that stimulates release of neurotransmitters. Topiramate also inhibits the activity of the excitatory neurotransmitter glutamate, which adds to the calming effect on brain electrical activity.

Gabapentin is an analogue of the inhibitory neurotransmitter GABA but does not work through the same receptors as GABA. It does however, bind to a receptor in brain neurones and is thought to control neurotransmission by blocking voltage-gated calcium channels, which reduces the propagation of excitatory nerve transmissions and calms excitatory nerve cells.

Bicarbonate

Acetazolamide inhibits the enzyme carbonic anhydrase, which catalyzes the rapid conversion of carbon dioxide to bicarbonate ions in many cells including nerve cells. Reducing the amount of bicarbonate ions helps control abnormal, paroxysmal (short frequent), excessive discharge (transmission of signal between nerve cells) from neurons that can cause convulsions such as in epilepsy.
...Read more

Transmission of nerve impulses

Messages are transmitted from one neurone (nerve cell) to another by the generation of electrical and chemical signals. At one end of the neurone, structures called dendrites pick up the stimulus from the connecting neurone and this generates an electrical signal that travels down the body of the cell called the axon and stimulates the release of chemical signals or neurotransmitters from the other end. These neurotransmitters travel across the gap or synapse between the axon terminal of one neurone (pre-synaptic) and the dendrites at the top of the next neurone (post-synaptic). They bind to specific receptors and trigger the generation of another electrical signal in the next neurone. This transmission of electrical and chemical messages takes just milliseconds to complete.

An electrical signal is generated by the exchange of charged particles or ions across voltage-dependant ion channels in the cell membrane controlled by ion pumps. When a neurone is not transmitting messages it is resting and its membrane is polarised which means that the electrical charge on the outside of the membrane is positive due to an excess of sodium ions, while the charge on the inside is negative and there is an excess of potassium ions.

When the neurone is stimulated, the gated channels on the membrane open and sodium ions flood into the cell and the membrane becomes depolarised generating an action potential and an electrical signal is propagated along the axon. The ions return to their original levels and the cell becomes repolarised, ready to receive another signal.

At the other end of the neurone, the electrical signal triggers the membrane to depolarise allowing calcium ions to enter the cell and this stimulates the release of neurotransmitters. Some neurotransmitters trigger an action potential in the next neurone and are is stimulatory, others are inhibitory and prevent the generation of an action potential. Once it has done its job the neurotransmitter is degraded or reabsorbed back into the pre-synaptic neurone that released it, so that the stimulus stops once transmission to the next neurone is complete.

What is epilepsy?

Epilepsy is characterised by recurring spontaneous seizures, which is uncontrolled muscular spasm, due to episodes of abnormal electrical activity in the brain. A chemical imbalance of neurotransmitters in the brain results in a malfunction in the transmission of electrical signals and causes repetitive firing and transmission of excitatory nerve messages. These bursts of abnormal electrical activity in the brain send nerve signals to the motor neurones in the central nervous system and trigger seizures. Epileptic seizures vary from mild convulsions to violent muscle spasms with loss of consciousness, depending on the part of the brain affected. The trigger for epileptic seizures can be due to anything that disturbs normal activity of neurones, including head injury, stroke, brain tumour, brain infection, drug abuse, but in many cases the cause is unknown (idiopathic) and epilepsy can start at any age.

Medications for epilepsy

Drugs used to prevent epileptic seizures are anticonvulsants that control the bursts of electrical activity in the brain that cause seizures. They work by preventing the repetitive firing of nerve messages acting through different mechanisms, including:

Blocking sodium channels that are involved in triggering the action potential and setting up the nerve signal

Blocking calcium channels that respond to the nerve signal and trigger the release of neurotransmitters

Adjusting the balance between inhibitory and excitatory neurotransmitters

Some medications work by more that one mechanism and act by a combination of these mechanisms.

Sodium/calcium channel blockers

Some anticonvulsants control neurotransmission and act directly on nerve cells to stabilise nerve cell membranes by blocking sodium or calcium channels. This reduces electrical activity and helps to “calm down” nerves that have become hyperexcited, thereby inhibiting the repetitive firing and transmission of excitatory nerve messages, in areas of the brain where hyperactivity causes seizures. Medications that act as membrane stabilisers include the following:

Carbamazepine blocks voltage-dependent sodium channels in nerve cell membranes that control the flow of sodium ions into the nerve cell and triggers an electrical transmission, which in hyperexcited nerve cells can trigger a seizure. This action is also thought to suppress the release of the neurotransmitters dopamine and noradrenaline.

Phenytoin acts directly on a specific area in the brain called the motor cortex, which controls movement and works by promoting the release of sodium ions out of the nerve cell through voltage-gated sodium channels in the membrane. This prevents the spread of electrical activity that sends nerve signals from the brain to the central nervous system to trigger a seizure.

Inhibitory and excitatory neurotransmitters

For the brain to function normally it is important to have a balance between excitatory and inhibitory neurotransmitters. Glutamate is the major excitatory neurotransmitter and interacts with receptors that have excitatory effects, which means that they increase the probability that the target cell will set up an action potential and trigger a nerve signal. Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter and interacts with receptors that have inhibitory effects by failing to trigger a nerve signal and this has a calming effect on nerve cells. Medications that regulate the balance between excitatory and inhibitory neurotransmitters include the following:

Sodium valproate increases the activity of the inhibitory neurotransmitter GABA. It works by inhibiting GABA degradative enzymes like GABA transaminase and/or succinic semialdehyde dehydrogenase thereby preventing its degradation; also by preventing the reuptake of GABA by the pre-synaptic nerve cell.

Topiramate stimulates the activity of GABA by enhancing the frequency that it activates its receptor; also by enhancing the ability of GABA to increase the flow of calcium ions into the end of the nerve cell that stimulates release of neurotransmitters. Topiramate also inhibits the activity of the excitatory neurotransmitter glutamate, which adds to the calming effect on brain electrical activity.

Gabapentin is an analogue of the inhibitory neurotransmitter GABA but does not work through the same receptors as GABA. It does however, bind to a receptor in brain neurones and is thought to control neurotransmission by blocking voltage-gated calcium channels, which reduces the propagation of excitatory nerve transmissions and calms excitatory nerve cells.

Bicarbonate

Acetazolamide inhibits the enzyme carbonic anhydrase, which catalyzes the rapid conversion of carbon dioxide to bicarbonate ions in many cells including nerve cells. Reducing the amount of bicarbonate ions helps control abnormal, paroxysmal (short frequent), excessive discharge (transmission of signal between nerve cells) from neurons that can cause convulsions such as in epilepsy.
...Read more

Our Migraine class of Neurological medications are used to treat migraine attack to relieve symptoms of migraine, including painful headache, with or without aura and visual disturbances, also nausea, and vomiting.

Use the search feature to quickly find the product you are looking for, by entering either the active ingredient, e.g. sumatriptan, or the product name, e.g. Imigran.

Our Migraine class of Neurological medications are used to treat migraine attack to relieve symptoms of migraine, including painful headache, with or without aura and visual disturbances, also nausea, and vomiting.

Use the search feature to quickly find the product you are looking for, by entering either the active ingredient, e.g. sumatriptan, or the product name, e.g. Imigran.

What is migraine?

Migraine is a neurological disorder with symptoms that include an intense, throbbing and painful headache, often accompanied by an aura, which is the perception of visual disturbances that appear as flashing lights or zig-zag lines and are usually the first sign that a migraine headache is on its way. A migraine is also associated with extreme sensitivity to light, sound, touch and smell. Other symptoms are gastrointestinal effects including nausea, vomiting and delayed emptying of the stomach into the small intestine, which reduces absorption of medications and can explain why oral medications are not effective fast enough. A migraine attack can last between four and 72 hours.

For many years migraine headache was considered to be a vascular headache and the primary cause was thought to be entirely due to constriction followed by extreme dilatation or widening of blood vessels in the head, with leakage of inflammatory chemicals, which in turn irritate nearby sensory nerves causing pain. With new developments in neuroscience, the current thinking is that migraine headache is a neurological disorder involving abnormalities in nerve pathways and brain chemicals or neurotransmitters. It is also now thought that there are distinct genes related to migraines and that there is a genetic component to developing migraines due to the presence of abnormal genes that control certain areas of the brain.

There are many possible migraine triggers, including, stress, hunger, lack of sleep, dietary factors, and hormonal changes such as during the menstrual cycle.

Migraine treatments

Medications for treatment of migraine currently focus on the vascular basis of migraine headache to prevent blood vessel widening by targeting two different neurotransmitters, serotonin and noradrenaline. These neurotransmitters act on specific receptors in the brain and control the stability of peripheral blood vessels in terms of dilation and constriction. Other medications are used for control of migraine symptoms by combining an analgesic and antiemetic.

Serotonin agonists

Serotonin is a brain chemical or neurotransmitter that is involved in control of mood, pain sensation, sexual behaviour, sleep, as well as dilation (widening) and constriction (narrowing) of blood vessels. Sumatriptan is a member of the group of drugs called tryptans and is a serotonin agonist that mimics the action of serotonin (also known as 5-hydroxytryptamine, or 5-HT). Sumatriptan acts specifically on the 5-HT1 receptor, which is a sub-type of the serotonin receptor that is found predominantly in the blood vessels of the brain, causing them to constrict or narrow. Sumatriptan is also thought to inhibit trigeminal nerve activity, relieving pain.

Treatment with sumatriptan should begin as soon as possible after symptoms begin and Injection is the fastest treatment for migraine relief, being effective within 10-15 minutes. A nasal spray is also available which delivers sumatriptan directly into the nasal passages where it is rapidly absorbed through the skin and is active within 15 minutes; this is particularly suitable if nausea and vomiting during a migraine attack make it difficult to take tablets. Sumatriptan is not fully absorbed so oral administration with tablets can take up to 30 minutes to relieve symptoms, although rapid release fast disintegration tablets are available to speed up absorption of sumatriptan. Sumatriptan does not prevent migraine attack and is not effective for other types of headache.

Alpha-agonists

Clonidine is an alpha-agonist that acts on alpha adrenergic receptors in the brain and central nervous system, which are usually stimulated by the neurotransmitter noradrenaline. Blood vessels in the brain have alpha adrenergic receptors and are responsive to adrenergic stimulation by the neurotransmitters adrenaline and noradrenaline. This stimulation causes the blood vessels to widen (vasodilation) or contract (vasoconstriction). Clonidine binds to alpha adrenergic receptors on peripheral blood vessels in the brain and this reduces their responsiveness to adrenergic stimuli and thereby controls the extreme dilatation that is thought to be associated with migraine headache.

Symptom relief

A combination of the analgesic paracetamol and the anti-emetic metoclopramide is used to help relieve symptoms of migraine, including pain, nausea, vomiting and gastric stasis, or delayed emptying of the stomach, which can slow down the absorption of migraine medication.

Paracetamol works by selectively inhibiting the enzyme cyclooxygenase 2 (COX-2) that is required for the production of prostaglandins, which are chemicals produced in response to inflammation and injury and can also sensitise nerve endings in the pain centres in the brain. Paracetamol blocks the production of pain-inducing prostaglandins, to relieve the pain associated with migraine headaches.

Metoclopramide is an antiemetic (prevents nausea and vomiting) and a gastrokinetic (stimulates gastrointestinal mobility). It acts as a dopamine antagonist by binding to dopamine receptors in specific areas in the brain where the vomiting reflex is stimulated and blocks the vomiting reflex. Metoclopramide also binds to dopamine receptors in the stomach, which mediates increased contraction of the stomach muscles so that the stomach empties faster and this reduces nausea and vomiting and increases the passage of the oral medication into the intestine for faster absorption.
...Read more

What is migraine?

Migraine is a neurological disorder with symptoms that include an intense, throbbing and painful headache, often accompanied by an aura, which is the perception of visual disturbances that appear as flashing lights or zig-zag lines and are usually the first sign that a migraine headache is on its way. A migraine is also associated with extreme sensitivity to light, sound, touch and smell. Other symptoms are gastrointestinal effects including nausea, vomiting and delayed emptying of the stomach into the small intestine, which reduces absorption of medications and can explain why oral medications are not effective fast enough. A migraine attack can last between four and 72 hours.

For many years migraine headache was considered to be a vascular headache and the primary cause was thought to be entirely due to constriction followed by extreme dilatation or widening of blood vessels in the head, with leakage of inflammatory chemicals, which in turn irritate nearby sensory nerves causing pain. With new developments in neuroscience, the current thinking is that migraine headache is a neurological disorder involving abnormalities in nerve pathways and brain chemicals or neurotransmitters. It is also now thought that there are distinct genes related to migraines and that there is a genetic component to developing migraines due to the presence of abnormal genes that control certain areas of the brain.

There are many possible migraine triggers, including, stress, hunger, lack of sleep, dietary factors, and hormonal changes such as during the menstrual cycle.

Migraine treatments

Medications for treatment of migraine currently focus on the vascular basis of migraine headache to prevent blood vessel widening by targeting two different neurotransmitters, serotonin and noradrenaline. These neurotransmitters act on specific receptors in the brain and control the stability of peripheral blood vessels in terms of dilation and constriction. Other medications are used for control of migraine symptoms by combining an analgesic and antiemetic.

Serotonin agonists

Serotonin is a brain chemical or neurotransmitter that is involved in control of mood, pain sensation, sexual behaviour, sleep, as well as dilation (widening) and constriction (narrowing) of blood vessels. Sumatriptan is a member of the group of drugs called tryptans and is a serotonin agonist that mimics the action of serotonin (also known as 5-hydroxytryptamine, or 5-HT). Sumatriptan acts specifically on the 5-HT1 receptor, which is a sub-type of the serotonin receptor that is found predominantly in the blood vessels of the brain, causing them to constrict or narrow. Sumatriptan is also thought to inhibit trigeminal nerve activity, relieving pain.

Treatment with sumatriptan should begin as soon as possible after symptoms begin and Injection is the fastest treatment for migraine relief, being effective within 10-15 minutes. A nasal spray is also available which delivers sumatriptan directly into the nasal passages where it is rapidly absorbed through the skin and is active within 15 minutes; this is particularly suitable if nausea and vomiting during a migraine attack make it difficult to take tablets. Sumatriptan is not fully absorbed so oral administration with tablets can take up to 30 minutes to relieve symptoms, although rapid release fast disintegration tablets are available to speed up absorption of sumatriptan. Sumatriptan does not prevent migraine attack and is not effective for other types of headache.

Alpha-agonists

Clonidine is an alpha-agonist that acts on alpha adrenergic receptors in the brain and central nervous system, which are usually stimulated by the neurotransmitter noradrenaline. Blood vessels in the brain have alpha adrenergic receptors and are responsive to adrenergic stimulation by the neurotransmitters adrenaline and noradrenaline. This stimulation causes the blood vessels to widen (vasodilation) or contract (vasoconstriction). Clonidine binds to alpha adrenergic receptors on peripheral blood vessels in the brain and this reduces their responsiveness to adrenergic stimuli and thereby controls the extreme dilatation that is thought to be associated with migraine headache.

Symptom relief

A combination of the analgesic paracetamol and the anti-emetic metoclopramide is used to help relieve symptoms of migraine, including pain, nausea, vomiting and gastric stasis, or delayed emptying of the stomach, which can slow down the absorption of migraine medication.

Paracetamol works by selectively inhibiting the enzyme cyclooxygenase 2 (COX-2) that is required for the production of prostaglandins, which are chemicals produced in response to inflammation and injury and can also sensitise nerve endings in the pain centres in the brain. Paracetamol blocks the production of pain-inducing prostaglandins, to relieve the pain associated with migraine headaches.

Metoclopramide is an antiemetic (prevents nausea and vomiting) and a gastrokinetic (stimulates gastrointestinal mobility). It acts as a dopamine antagonist by binding to dopamine receptors in specific areas in the brain where the vomiting reflex is stimulated and blocks the vomiting reflex. Metoclopramide also binds to dopamine receptors in the stomach, which mediates increased contraction of the stomach muscles so that the stomach empties faster and this reduces nausea and vomiting and increases the passage of the oral medication into the intestine for faster absorption.
...Read more

What is Parkinson’s?

Parkinson’s disease is a degenerative neurological motor system disorder caused by gradual loss of specific dopamine-producing neurones (nerve cells) in the area of the mid-brain called the substantia nigra. Dopamine is a neurotransmitter that plays an important role in controlling muscle function and movement. It links several nerve pathways involved in various brain functions, including motor function, memory, learning and decision making. The loss of communication between the various areas of the brain due to reduced levels of dopamine is associated with the symptoms of Parkinson’s, most of which are related to abnormal movement. Symptoms of Parkinson’s include, uncontrolled trembling in hands, arms, legs, jaw, and face (tremor); overall stiffness if the body and limbs; slowness of movement (bradykinesia) and impaired balance and coordination. As the disease progresses, symptoms become more pronounced and develop into difficulty with walking, talking and swallowing; as well as urinary or bowel problems, sleeping problems and depression. Parkinsonism is the term used to describe a group of movement disorders, which produce the same signs and symptoms as Parkinson’s disease but have known causes, including, stroke and side effect of medication, particularly neuroleptics, antipsychotics and narcotic overdose.

Medications for Parkinson’s

Medications used to treat Parkinson’s disease focus on the loss of dopamine in the brain and increase the amount of dopamine by different mechanisms. These medications provide symptom relief but cannot cure the disease. Medications that increase dopamine include:

Levodopa, in combination with carbidopa, that substitute for dopamine

Amantadine, that increases dopamine availability

Selegiline, that prevents degradation of dopamine

Bromocriptine, that acts as a dopamine agonist

Other medications like Orphenadrine and Amantadine relieve symptoms due to their anticholinergic activity.

Restoring dopamine levels

Levodopa is the metabolic precursor of dopamine and is converted to dopamine in the brain by the enzyme decarboxylase. Carbidopa is a decarboxylase inhibitor but does not cross the blood brain barrier, so that when administered together with levodopa it prevents its conversion in the blood until it reaches the brain. This action ensures that more levodopa gets into the brain for conversion to dopamine to help restore dopamine levels in the brain.

Increasing dopamine availability

A neurotransmitter like dopamine is released by the pre-synaptic neurone, crosses the synapse and binds to receptors on the post-synaptic neurone, where it activates a nerve signal and thereby propagates the transmission of nerve signals. Any remaining neurotransmitter in the synapse is degraded by specific enzymes and/or reused by re-uptake into the pre-synaptic neurone. Each stage of this process is a potential target for drug intervention that can increase the availability of a neurotransmitter like dopamine.

Monoamine oxidase (MAO) is an enzyme that inactivates certain neurotransmitters, including dopamine, after they have transmitted nerve signals from one neurone to the next. Selegiline is a selective inhibitor of the MAO type B enzyme that is found in neurones and causes the degradation of dopamine. Selegiline has several actions to promote dopamine availability; it prevents breakdown of dopamine and inhibits the re-uptake of dopamine from the synapse. It also blocks pre-synaptic dopamine receptors, which may help increase the activity of dopamine in the brain. Selegiline has been found to be effective in reducing symptoms in early stages of Parkinson’s disease, but is also used in combination with levodopa to help control symptoms as the condition progresses and worsens and it is thought to potentiate the effectiveness of levodopa.

Amantadine is another drug that increases dopamine availability in the brain. It acts by enhancing the release of dopamine into the synapse and by delaying its re-uptake from the synapse.

Stimulating dopamine receptors

Bromocriptine is a dopamine agonist that binds to dopamine receptors in various parts of the brain and activates dopamine-stimulated pathways. Stimulation of the dopamine receptors in the brain mimics the effect of dopamine and is helpful in treating symptoms of Parkinson’s disease.

Anticholinergics

Acetylcholine is a neurotransmitter that has several excitatory functions, including activating skeletal muscle contraction. Drugs that block the receptors for acetylcholine are known as anticholinergic and include amantadine and orphenadrine. Drugs with anticholinergic activity can be used to help prevent the involuntary movements associated with Parkinson’s disease.
...Read more

What is Parkinson’s?

Parkinson’s disease is a degenerative neurological motor system disorder caused by gradual loss of specific dopamine-producing neurones (nerve cells) in the area of the mid-brain called the substantia nigra. Dopamine is a neurotransmitter that plays an important role in controlling muscle function and movement. It links several nerve pathways involved in various brain functions, including motor function, memory, learning and decision making. The loss of communication between the various areas of the brain due to reduced levels of dopamine is associated with the symptoms of Parkinson’s, most of which are related to abnormal movement. Symptoms of Parkinson’s include, uncontrolled trembling in hands, arms, legs, jaw, and face (tremor); overall stiffness if the body and limbs; slowness of movement (bradykinesia) and impaired balance and coordination. As the disease progresses, symptoms become more pronounced and develop into difficulty with walking, talking and swallowing; as well as urinary or bowel problems, sleeping problems and depression. Parkinsonism is the term used to describe a group of movement disorders, which produce the same signs and symptoms as Parkinson’s disease but have known causes, including, stroke and side effect of medication, particularly neuroleptics, antipsychotics and narcotic overdose.

Medications for Parkinson’s

Medications used to treat Parkinson’s disease focus on the loss of dopamine in the brain and increase the amount of dopamine by different mechanisms. These medications provide symptom relief but cannot cure the disease. Medications that increase dopamine include:

Levodopa, in combination with carbidopa, that substitute for dopamine

Amantadine, that increases dopamine availability

Selegiline, that prevents degradation of dopamine

Bromocriptine, that acts as a dopamine agonist

Other medications like Orphenadrine and Amantadine relieve symptoms due to their anticholinergic activity.

Restoring dopamine levels

Levodopa is the metabolic precursor of dopamine and is converted to dopamine in the brain by the enzyme decarboxylase. Carbidopa is a decarboxylase inhibitor but does not cross the blood brain barrier, so that when administered together with levodopa it prevents its conversion in the blood until it reaches the brain. This action ensures that more levodopa gets into the brain for conversion to dopamine to help restore dopamine levels in the brain.

Increasing dopamine availability

A neurotransmitter like dopamine is released by the pre-synaptic neurone, crosses the synapse and binds to receptors on the post-synaptic neurone, where it activates a nerve signal and thereby propagates the transmission of nerve signals. Any remaining neurotransmitter in the synapse is degraded by specific enzymes and/or reused by re-uptake into the pre-synaptic neurone. Each stage of this process is a potential target for drug intervention that can increase the availability of a neurotransmitter like dopamine.

Monoamine oxidase (MAO) is an enzyme that inactivates certain neurotransmitters, including dopamine, after they have transmitted nerve signals from one neurone to the next. Selegiline is a selective inhibitor of the MAO type B enzyme that is found in neurones and causes the degradation of dopamine. Selegiline has several actions to promote dopamine availability; it prevents breakdown of dopamine and inhibits the re-uptake of dopamine from the synapse. It also blocks pre-synaptic dopamine receptors, which may help increase the activity of dopamine in the brain. Selegiline has been found to be effective in reducing symptoms in early stages of Parkinson’s disease, but is also used in combination with levodopa to help control symptoms as the condition progresses and worsens and it is thought to potentiate the effectiveness of levodopa.

Amantadine is another drug that increases dopamine availability in the brain. It acts by enhancing the release of dopamine into the synapse and by delaying its re-uptake from the synapse.

Stimulating dopamine receptors

Bromocriptine is a dopamine agonist that binds to dopamine receptors in various parts of the brain and activates dopamine-stimulated pathways. Stimulation of the dopamine receptors in the brain mimics the effect of dopamine and is helpful in treating symptoms of Parkinson’s disease.

Anticholinergics

Acetylcholine is a neurotransmitter that has several excitatory functions, including activating skeletal muscle contraction. Drugs that block the receptors for acetylcholine are known as anticholinergic and include amantadine and orphenadrine. Drugs with anticholinergic activity can be used to help prevent the involuntary movements associated with Parkinson’s disease.
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About the nervous system

The brain is the control centre for the nervous system; it receives information from the outside world and controls all our responses to incoming information. It is divided into different areas responsible for different aspects of our body function and actions, including behaviour, movement, feelings, memory and learning. The spinal cord travels down the spinal column, protected by the vertebrae carrying messages to and from the brain. It has many branches forming the major nerves, which themselves branch many times to service all parts of the body. The brain and spinal cord form the central nervous system (CNS) and the nerves form the peripheral nervous system.

The nervous system is made up of nerve cells or neurones, which communicate with each other by transmitting electrical impulses from one neurone to another. Neurones are separated by gaps or synapses and the electrical signal is transmitted across the synapse by the release of a neurotransmitter or brain chemical from the pre-synaptic neurone; neurotransmitter, which then binds to specific receptors in the post-synaptic neurone. This is how information is collected by sensory organs and transmitted via sensory neurones to the brain for processing. The response is transmitted by motor neurones to the muscles and glands for appropriate action.

Neurotransmitters

There are several different types of neurotransmitter that control the various neural pathways. Neurotransmitters work through specific receptors and are commonly referred to as excitatory or inhibitory, depending on whether or not binding to its receptor activates an electrical signal in the next neurone. Some have the ability to be either excitatory or inhibitory and their role depends on what type of response they induce in the nervous system.

Gamma aminobutyric acid (GABA) is generally considered the major inhibitory neurotransmitter in the brain. Lack of GABA is thought to be associated with epilepsy.

Glutamate is generally considered the major excitatory neurotransmitter in the brain.

Acetylcholine has several excitatory functions including activating skeletal muscle contraction. It also works through various different receptors in the brain, where it is involved in memory and learning. Loss of these cells is associated with Alzheimer’s.

Dopamine plays an important role in mood and is the “feel good” neurotransmitter as it s involved in the reward circuits of the brain. It also plays an important role in controlling muscle function and movement. Loss of dopamine receptive brain cells is associated with Parkinson’s disease.

Serotonin plays an important role in regulation of many pathways in the brain, including the control of mood, sleep, body temperature, pain and appetite.

Noradrenaline in the brain plays an important role in regulation of attention and arousal. In the central nervous system it is involved in the “fight or flight” response, which affects heart rate, blood pressure and gastrointestinal activity.

What is a neurological disorder?

A neurological disorder is caused by a malfunction of the nervous system, which includes the brain, spinal cord, and nerves. Since the nervous system controls all aspects of bodily function and actions, any damage will have some serious symptoms. These may be impaired motor function including, paralysis, uncoordinated movements and seizures; impaired sensory function, including pain and loss of sensation; impaired cognitive function, including confusion, memory loss, emotional and behavioural disturbances.

Types of neurological disorder

The symptoms of a neurological disorder can be due to a genetic defect resulting in an inherited disorder, damage or trauma to the nervous system or due to the aging process. Types of neurological disorder include:

Degenerative neurological conditions resulting in destruction of specific areas of the brain so that symptoms manifest and worsen progressively over time, for example, Parkinson’s disease and Alzheimer’s.

A malfunction in brain activity resulting in uncontrolled muscular spasm known as seizures; if these occur regularly, the condition is called epilepsy.

Abnormal release of neurochemicals that cause inflammation, extreme widening of blood vessels in the brain, which press on nearby nerves and induces pain and other symptoms of a migraine headache; it is thought to be related to abnormal genes that control certain areas of the brain.

Motion sickness

A discrepancy between sensory input from the eyes and the organs in the ears that perceive movement causes confusion in the brain, which leads to motion sickness. This is a neurological condition that is based on perception rather than a physical disorder.

Treatments for neurological disorders

Often there is no effective preventative treatment or cure for neurological disorders and most available treatments are aimed at relieving or reducing symptoms. Treatments include:

Neurotransmitter receptors blockers, such as acetylcholine receptors used in the treatment of motion sickness.

Preventing breakdown of important neurotransmitters like acetylcholine in the treatment Alzheimer's Disease.

Anticonvulsants that by work by various mechanisms including stabilizing nerve cell membranes and changing levels of neurotransmitters; these are used to treat epilepsy.

Increasing the amount of dopamine by various mechanisms used for treatment of Parkinson’s disease.

Muscle relaxants that work by blocking acetylcholine used for treatment of Parkinson’s disease.

About the nervous system

The brain is the control centre for the nervous system; it receives information from the outside world and controls all our responses to incoming information. It is divided into different areas responsible for different aspects of our body function and actions, including behaviour, movement, feelings, memory and learning. The spinal cord travels down the spinal column, protected by the vertebrae carrying messages to and from the brain. It has many branches forming the major nerves, which themselves branch many times to service all parts of the body. The brain and spinal cord form the central nervous system (CNS) and the nerves form the peripheral nervous system.

The nervous system is made up of nerve cells or neurones, which communicate with each other by transmitting electrical impulses from one neurone to another. Neurones are separated by gaps or synapses and the electrical signal is transmitted across the synapse by the release of a neurotransmitter or brain chemical from the pre-synaptic neurone; neurotransmitter, which then binds to specific receptors in the post-synaptic neurone. This is how information is collected by sensory organs and transmitted via sensory neurones to the brain for processing. The response is transmitted by motor neurones to the muscles and glands for appropriate action.

Neurotransmitters

There are several different types of neurotransmitter that control the various neural pathways. Neurotransmitters work through specific receptors and are commonly referred to as excitatory or inhibitory, depending on whether or not binding to its receptor activates an electrical signal in the next neurone. Some have the ability to be either excitatory or inhibitory and their role depends on what type of response they induce in the nervous system.

Gamma aminobutyric acid (GABA) is generally considered the major inhibitory neurotransmitter in the brain. Lack of GABA is thought to be associated with epilepsy.

Glutamate is generally considered the major excitatory neurotransmitter in the brain.

Acetylcholine has several excitatory functions including activating skeletal muscle contraction. It also works through various different receptors in the brain, where it is involved in memory and learning. Loss of these cells is associated with Alzheimer’s.

Dopamine plays an important role in mood and is the “feel good” neurotransmitter as it s involved in the reward circuits of the brain. It also plays an important role in controlling muscle function and movement. Loss of dopamine receptive brain cells is associated with Parkinson’s disease.

Serotonin plays an important role in regulation of many pathways in the brain, including the control of mood, sleep, body temperature, pain and appetite.

Noradrenaline in the brain plays an important role in regulation of attention and arousal. In the central nervous system it is involved in the “fight or flight” response, which affects heart rate, blood pressure and gastrointestinal activity.

What is a neurological disorder?

A neurological disorder is caused by a malfunction of the nervous system, which includes the brain, spinal cord, and nerves. Since the nervous system controls all aspects of bodily function and actions, any damage will have some serious symptoms. These may be impaired motor function including, paralysis, uncoordinated movements and seizures; impaired sensory function, including pain and loss of sensation; impaired cognitive function, including confusion, memory loss, emotional and behavioural disturbances.

Types of neurological disorder

The symptoms of a neurological disorder can be due to a genetic defect resulting in an inherited disorder, damage or trauma to the nervous system or due to the aging process. Types of neurological disorder include:

Degenerative neurological conditions resulting in destruction of specific areas of the brain so that symptoms manifest and worsen progressively over time, for example, Parkinson’s disease and Alzheimer’s.

A malfunction in brain activity resulting in uncontrolled muscular spasm known as seizures; if these occur regularly, the condition is called epilepsy.

Abnormal release of neurochemicals that cause inflammation, extreme widening of blood vessels in the brain, which press on nearby nerves and induces pain and other symptoms of a migraine headache; it is thought to be related to abnormal genes that control certain areas of the brain.

Motion sickness

A discrepancy between sensory input from the eyes and the organs in the ears that perceive movement causes confusion in the brain, which leads to motion sickness. This is a neurological condition that is based on perception rather than a physical disorder.

Treatments for neurological disorders

Often there is no effective preventative treatment or cure for neurological disorders and most available treatments are aimed at relieving or reducing symptoms. Treatments include:

Neurotransmitter receptors blockers, such as acetylcholine receptors used in the treatment of motion sickness.

Preventing breakdown of important neurotransmitters like acetylcholine in the treatment Alzheimer's Disease.

Anticonvulsants that by work by various mechanisms including stabilizing nerve cell membranes and changing levels of neurotransmitters; these are used to treat epilepsy.

Increasing the amount of dopamine by various mechanisms used for treatment of Parkinson’s disease.

Muscle relaxants that work by blocking acetylcholine used for treatment of Parkinson’s disease.